| Direct inhibition by angiotensin II of insulin-dependent glucose transport activity in mammalian skeletal muscle involves a ROS-dependent mechanism. | |
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MedLine Citation:
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PMID: 20384568 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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No previous study has investigated how the vaso-constrictive peptide Ang II impacts insulin action in isolated mammalian skeletal muscle. We investigated the molecular actions of Ang II on insulin signalling and glucose transport in skeletal muscle from lean Zucker rats. Soleus strips were incubated with insulin (5 mU/ml) and/or Ang II (500 nM) for 2 hours. Ang II caused significant (p < 0.05) inhibition of insulin-stimulated glucose transport (39%) and decreased phosphorylation of Akt Ser(473) (37%) and glycogen synthase kinase-3beta Ser(9) (42%) without affecting phosphorylation of IRS-1 Ser(307) or p38 MAPK. We used the superoxide dismutase mimetic, tempol (1 mM), to determine if reactive oxygen species (ROS) contribute to Ang II-mediated insulin resistance. Tempol partially reversed (42%) Ang II-induced inhibition of insulin-stimulated glucose transport. These results indicate that Ang II inhibits distal insulin signalling and insulin-stimulated glucose transport in isolated mammalian skeletal muscle, and that this effect is partially mediated by ROS. |
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Authors:
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Maggie K Diamond-Stanic; Erik J Henriksen |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural |
Journal Detail:
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Title: Archives of physiology and biochemistry Volume: 116 ISSN: 1744-4160 ISO Abbreviation: Arch. Physiol. Biochem. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-27 Completed Date: 2010-07-21 Revised Date: 2012-03-15 |
Medline Journal Info:
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Nlm Unique ID: 9510153 Medline TA: Arch Physiol Biochem Country: England |
Other Details:
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Languages: eng Pagination: 88-95 Citation Subset: IM |
Affiliation:
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Muscle Metabolism Laboratory, Department of Physiology and Arizona Diabetes Program, University of Arizona College of Medicine, Tucson, AZ 85721-0093, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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metabolism,
pharmacology* Animals Biological Transport Female Glucose / metabolism, pharmacology Hypoglycemic Agents / metabolism, pharmacology Insulin / metabolism*, pharmacology MAP Kinase Kinase Kinases Mammals / metabolism Muscle, Skeletal / drug effects, metabolism Phosphorylation / drug effects Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt / metabolism Rats Rats, Zucker Reactive Oxygen Species / metabolism*, pharmacology Signal Transduction / drug effects p38 Mitogen-Activated Protein Kinases / metabolism, pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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DK063967/DK/NIDDK NIH HHS; R01 DK063967-01A2/DK/NIDDK NIH HHS; T32 HL07249/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hypoglycemic Agents; 0/Insulin; 0/Proto-Oncogene Proteins; 0/Reactive Oxygen Species; 11128-99-7/Angiotensin II; 50-99-7/Glucose; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25/MAP Kinase Kinase Kinases; EC 2.7.11.25/MAP3K8 protein, human |
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